Category: Diabetes 101

A biochemist at Rice University claims that there may be a link between autism and Type 2 diabetes since the two disorders share common biochemical and genetic markers.

“It appears that both Type 2 diabetes and autism have a common underlying mechanism — impaired glucose tolerance and hyperinsulinemia,” wrote Dr. Michael Stern in an opinion paper published in a recent issue of the journal “Frontiers in Cellular Endocrinology.”

Hyperinsulinemia is a condition in which insulin levels in the bloodstream remain elevated. Both obesity and Type 2 diabetes are associated with insulin resistance, and hyperinsulinemia often precedes insulin resistance.

“It will be very easy for clinicians to test my hypothesis,” said Stern, who teaches cell biology and biochemistry at Rice University. “They could do this by putting autistic children on low-carbohydrate diets that minimize insulin secretion and see if their symptoms improve.”

Dr. Stern also noted that, if hyperinsulinemia is positively associated with autism, it would warrant more thorough testing of glucose tolerance in pregnant women.

According to Stern, he first hypothesized that autism and Type 2 diabetes could be linked by common factors several years ago, but assumed that someone else had already established the link.

Stern conducts his research at his lab, located at Rice University’s BioScience Research Collective, where he focuses on investigating genetic links between genetic disorders such as neurofibromatosis—which significantly increases risk of autism and autism spectrum disorders, such as Asperger’s syndrome.

According to the U.S. Centers for Disease Control and Prevention, autism spectrum disorders affect about nine out of every 1,000 children in the U.S. Autism and its related disorders are largely based in genetics, but scientists still do not clearly understand their genetic associations.

The biochemical pathway called PI3K/Tor is known to be linked with autism, since at least four genes associated with increased risk of autism produce proteins that play key roles in the pathway. Stern had previously been studying an abnormality in the synapses of fruit flies that appeared similar to abnormalities in mice and rats who demonstrated defects associated with the mGluR-mediated long-term depression pathway.

“I had also spent a lot of time thinking about insulin signaling because another project in my lab is an endocrinology project in which we’re studying how key proteins involved in insulin signaling affect the timing of metamorphosis in fruit flies,” said Stern.

Stern’s work allowed him to see the relationship between diabetes and autism: he knew that the PI3K/Tor pathway was responsible for intracellular insulin signals and he knew that insulin could affect synapses the same way that defects in the mGluR pathway could affect them. However, he didn’t immediately test or publish his hypothesis.

“When I read that the incidence of autism was increasing, and combined that with the fact that the incidence of Type 2 diabetes is also increasing, it seemed reasonable that each increase could have the same ultimate cause — the increase in hyperinsulinemia in the general population,” he said.  “I didn’t do anything with this notion for a few years because it seemed so obvious that I figured everyone already knew this hypothesis, or had tested it and found it was not true.”

Stern believes that the possible effects of insulin on neural disorders warrants more study.

“Based on what’s already in the literature, insulin needs to be taken seriously as a causative element in autism,” he said. “I hope that clinicians will take the next step and put this to a rigorous test and determine how to best use this information to benefit patients.”

A $32.3 million rescue package has revitalized a revolutionary kind of Type 1 diabetes treatment that was on the ropes financially. The treatment uses transplanted pig cells to treat Type 1 diabetes and with the new cash infusion, the developers claim that the product will be on the market in New Zealand within three years’ time.

The treatment has been in development by Living Cell Technologies for over two decades and is supposed to eliminate the need for regular insulin injections among Type 1 diabetics in addition to reducing the chances of severe complications or death resulting from the disease. According to Bob Elliott, acting chief executive of Living Cell, the company was facing such a dire cash shortage that it would have closed by the end of the year.

“We had three to four months left of liquid capital,” said Elliott. “The balance sheet told you the company was going to go out of existence at around Christmas time.”

Living Cell recently announced a new deal with Otsuka Pharmaceutical Factory, a large Japanese collective that manufactures a variety of health-related products, from cancer medications and sports drinks. Otsuka is responsible for a $32.3 million cash injection to keep Living Cell afloat. Otsuka and Living Cell were already partners, but the new deal will grant Otsuka a half share of the diabetes treatment and establishes a joint venture between the two companies.

Elliott stated that not only would the partnership allow Living Cell to complete work on its diabetes treatment and have it ready for market within a few years, but it would also allow the company to ramp up work on another project—a treatment for Parkinson’s disease.

“The purpose of the joint venture is to bring the diabetes treatment to being available for treatment rather than clinical trials,” said Elliott. “There is still about two to three years of further clinical trials required to refine our process, including dose schedules, before getting the product registered.”

Living Cell’s revolutionary treatment uses pancreatic beta cells extracted from piglets. The cells and transplanted into the abdomen of an individual with Type 1 diabetes, where they begin secreting insulin in response to elevated blood glucose levels, just as normal pancreatic beta cells do. The treatment also does not require the use of immunosuppression drugs to combat tissue rejection since it encapsulates cell clusters.

Although Elliott is grateful for the cash infusion, he says that it came as somewhat of a surprise. “We’ve got somebody with substantial money coming in behind us. They see it as a good business. They are attracted to it because a couple of members of the Otsuka family have type 1 diabetes,” he said.

Researchers at Living Cell have already conducted successful trials of the treatment in humans in Russia and Auckland, New Zealand. They have also begun testing in Argentina.

Once those studies are complete and Living Cell researchers have a chance to optimize cell transplant doses, they will conduct one more series of clinical trials beginning next year. Once those trials are complete, the company will seek licenses to market the therapy internationally.

The trials conducted so far have produced successful findings: patients in the Russian trial reducing their dependency on insulin injections and the treatment successfully combated a condition in the Auckland patients in which they experienced severely low blood glucose levels. Results were varied, but the majority of patients demonstrated improvements in reliance on insulin injection and overall diabetes control.

Weight loss surgery appears to have benefits beyond reducing obesity—a key risk factor for Type 2 diabetes—in one individual. Surgery also promotes weight loss, healthy eating habits, and increased levels of physical activity among the family members of surgery recipients.

A prospective, longitudinal study conducted by Dr. Gavitt A. Woodard and colleagues at Stanford University in California found that weight loss from this type of surgery appears to be “socially contagious,” inducing positive changes in nearby individuals.

“Previous studies have shown that obesity may be a social contagion and that by associating with obese individuals, a person is more likely to become obese. Our study may demonstrate that bariatric surgery in selected populations can provide a reverse corollary and induce weight loss and healthy behaviors in people surrounding the patient,” said Dr. Woodard.

Dr. Woodard’s team studied weight loss and lifestyle changes in close family—parents, spouses, and children—of those who had received Roux-en-Y gastric bypass surgery, a type of bariatric weight loss surgery. In all, 35 families were studied, including 35 surgery patients, 26 spouses, 3 grandparents, 6 adult children, and 15 children under the age of 18. The study was conducted over a two year period.

Both patients and family members attended educational sessions before and after the surgery. Patients were advised to eat a controlled diet of six meals per day, at 200-300 calories each. They were also advised to make lifestyle changes such as increasing physical activity to 10,000 steps per day, getting eight hours of sleep per night, limiting alcohol intake, and refraining from watching television for more than two hours per day.

A year after the surgeries were conducted, study participants were given physical examinations as well as questionnaires to determine any lifestyle changes, including those related to quality of life, overall health, sleep patterns, level of physical activity, and amount of television viewing.

Unsurprisingly, the patients undergoing surgery lost weight. However, family members lost weight as well: mean weight of adult family members decreased to 198 pounds from 220. That difference was not statistically significant until the researchers adjusted for baseline weight in each patient, which revealed significant changes.

Obese family members demonstrated significant weight loss, their mean weight dropping from 234 pounds to 226 pounds. Non-obese adults dropped from 180 to 176 pounds, but that difference was not statistically significant. Decreases in body mass index followed the same pattern, as did decreases in waist circumference: obese adult family members decreased in mean waist circumference from 119cm to 111cm. Non-obese family members, meanwhile, did not show a significant decrease.

The findings demonstrate that living with a family member who has undergone weight loss surgery appears to be as effective for weight loss as following one of several popular diets, including the Atkins, Zone, LEARN, or Ornish diets. Obese family members lost 3 percent of their total weight at the one-year follow-up, which falls within the 2 to 5 percent typically associated with those diets.

“Living with a gastric bypass patient and undertaking a structured diet plan along with the patient may have an equivalent effect on weight,” wrote the research team.

Family members also showed improvements in lifestyle, especially in eating habits, reporting less emotional eating and uncontrolled eating. Researchers also commented that family members displayed increased “cognitive control of eating.” Consumption of alcohol significantly decreased, from 5 drinks per month for patients to 0.2 and from 11 per month for family members to 0.8 per month.

The research team concluded that “bariatric surgery provides an opportunity for intervention for many individuals beyond the patient.”

A recent Norwegian study found that lung cancer patients who also have diabetes often live longer than patients who do not have diabetes. The study was published in the “Journal of Thoracic Oncology,” the official journal associated with the International Association for the Study of Lung Cancer.

The research team did not offer any theories about the underlying mechanism that causes the relationship, but did note that additional research was warranted. Additionally, they commented that the relationship did not constitute a justification for withholding standard cancer treatment from individuals with diabetes.

“Standard therapy should not be withheld from patients with diabetes mellitus provided they are otherwise fit, even if it may be considered a significant comorbidity,” wrote the researchers. “The survival benefit may be of clinical importance and should be focused on in future studies,” they added.

The study was conducted jointly by the Norwegian University of Science and Technology and Trondheim University. Researchers analyzed data from 1,677 lung cancer patients across three studies: the Nord-Trøndelag Health study (HUNT), the pemetrexed gemcitabine (PEG) study, and the Norwegian Lung Cancer Biobank study. The investigation was the first of its kind, being a cohort study confined to a particular geographical area with a large and stable population which looked at possible links between diabetes, lung cancer, and patient survival rates.

The researchers found that, in patients with both lung cancer and diabetes, survival rates were consistently higher across the follow-up period. After one year, survival in patients with lung cancer and diabetes was 43 percent compared to 28 percent without diabetes; at two years, survival rates were 19 percent compared to 11 percent; and at three years, survival rates were 3 percent compared to 1 percent.

The research team noted that the lower incidence of metastatic diseases in patients with diabetes could partly explain the unexpected differences in survival rates:

“The fact that patients with diabetes mellitus showed a lower frequency of metastatic diseases may partly explain the survival benefit in patients with diabetes mellitus, because the majority of the patients with lung cancer die of metastasis and not of the primary tumor,” they wrote.

After the researchers adjusted for the severity of diseases, however, it became clear that diabetes patients survived longer. Even patients with advanced lung cancer survived longer when they had diabetes.

“However, as we adjusted for stage of disease in our analyses this potential advantage can hardly explain the observed increased survival in patients with diabetes mellitus. In addition, increased survival in patients with diabetes mellitus was clearly demonstrated in the PEG study where all patients had advanced lung cancer.”

“Patients with lung cancer with diabetes mellitus have an increased survival compared with those without diabetes mellitus,” concluded the research team.

Lung cancer is the most dangerous form of cancer in the United States, claiming more lives than any other type, in both men and women. In 2007, over 200,000 patients received diagnoses of lung cancer, while over 150,000 died from the disease. Still, lung cancer rates have been decreasing in men for years while slowly rising in women. According to the American Cancer Society, risk of developing cancer for men is about 1 in 13, while risk for women is about 1 in 16. Lung cancer affects both smokers and non-smokers, although risk significantly increases in smokers. Lung cancer is typically a very serious diagnosis, though about 400,000 people today have been diagnosed with lung cancer and beat the disease.

Neural stem cells may someday be used to replace the beta cells of the pancreas that are destroyed by diabetes, according to a Japanese research team. The findings, which were published in a recent issue of the journal “EMBO Molecular Medicine,” demonstrate how the shortage of transplantable, donated beta cells could be overcome by using stem cells to regenerate an individual’s own beta cells.

Affecting over 200 million people around the world, diabetes is caused by decreased insulin production in the pancreas—specifically, in the beta cells of the pancreas. No cure for the disease exists today, so patients must rely on supplemental insulin treatment or other therapeutics to ensure that blood glucose levels remain regulated.

The research team was headed by Dr. Tomoko Kuwabara with the AIST Institute in Tsubuka, Japan. Dr. Kuwabara’s team focused developing new ways to control stem cell differentiation in humans, which would allow scientists to transplant stem cells and give them instructions to regrow any type of cell in the human body, such as pancreatic beta cells.

Dr. Kuwabara commented that since diabetes is caused by a lack of only one type of cell, it makes a good candidate for treatment with stem cells. “As diabetes is caused by the lack of a single type of cell the condition is an ideal target for cell replacement treatments,” he said. “However donation shortages of pancreatic beta cells are a major hurdle to advancing this treatment. So a safe and easy way of using stem cells for obtaining new beta cells has been long awaited.”

Dr. Kuwabara’s team used cells from the hippocampus and olfactory bulbs—regions of the brain that scientists can easily access to obtain transplantable cells. These brain cells do not normally produce insulin in the capacity that beta cells do. However, when the neuronal cells were transplanted into diabetic rats, they began to express important characteristics normally seen in the beta cells of the pancreas. They also began to produce more insulin, resulting in a decrease of average blood glucose levels. When the transplanted cells were removed, blood glucose levels increased, revealing that the cells were responsible for the positive changes. According to the research team, this method of transplanting brain cells into the pancreas could prove to be an effective treatment for diabetes that focuses on addressing the lack of beta cells rather than medicating insulin or blood glucose levels.

“The discovery of stem cells which have virtually unlimited self-renewal raises great expectations for their use in regenerative medicine,” wrote Onur Basak and Hans Clevers, who published a close up paper in the same issue of EMBO Molecular Medicine.

“The isolation and cultivation of stem cells as a renewable source of beta cells would be a major breakthrough,” they continued.

Basak and Clevers added: “Dr Kuwabara’s team found that transplanting neural stem cells directly into the pancreas can unleash their intrinsic ability to act as critical regulators of insulin production, and most importantly they demonstrated that the cells could be gained from a patient without the need for genetic manipulation.”

“Our findings demonstrate the potential value of neural stem cells for treating diabetes without gene transfer,” said Dr. Kuwabara. “This presents an original strategy to overcome the donor shortage which has hindered cell replacement therapy.”

Physicians have known for decades that regular physical activity is one of the key methods of diabetes prevention, as it prevents obesity—one of the key risk factors in developing Type 2 diabetes. A new program is attempting to bring that message to children by encouraging children to dance away their risk of diabetes.

The “Dance for Health” program is put on by the University of Pennsylvania School of Nursing along with Sayre High School of Philadelphia and the Bernett Johnson Sayre Health Center. The program aims to help assess physical activity levels among school-age children and encourage them to engage in more physical activity, with the ultimate goal of reducing obesity. The program is headed by Dr. Terri Lipman, Ph.D., CRNP, of the University of Pennsylvania School of Nursing; Dr. Lipman first established the partnership between the School of Nursing and Sayre High School in 2005.

The program sees the dance team of Sayre High School leading children in an hour of dancing, once a week for a month. Researchers associated with the program use pedometers to evaluate the physical activity levels of the children, finding that they took about twice as many steps on the days that they participated in the Dance for Health program.

The children did, however, display elevated resting heart rates, even after they stopped exercise—a sign of a lack of physical fitness. Dr. Lipman hopes that the program will teach the children to engage in more frequent physical activity and improve their overall health.

“Dancing is not only free, culturally relevant, and fun, it is also an easily accessible way for children to lead a more active lifestyle,” said Dr. Lipman. “Through this program, we aim to promote to schools and health care providers the benefits of incorporating dance into children’s lives to improve their overall health.”

According to Dr. Lipman, the program’s helpful benefits have extended beyond just the children attending the dance sessions. The partnership between the School of Nursing and Sayre High School has allowed nurse practitioner students the opportunity to educate nearby communities—which are at a high risk of diabetes—on the importance of eating right, exercising frequently, and identifying warning signs in the prevention of diabetes. The partnership allows nurse practitioners to conduct basic tests such as weight, height, and waist circumference, in addition to checking for acanthosis nigricans—a condition associated with diabetes in which areas of the skin become darkened.

“Our partnership with Sayre has opened the door to a strong relationship with residents of the community around Penn,” said Dr. Lipman. “It has allowed us to work with individuals, schools, and community groups to fight diabetes together.”

The School of Nursing at the University of Pennsylvania is known as a leading research institution in the field of nursing; areas of specialty include oncology, pediatrics, geriatrics, and quality-of-life choices. The National Institutes of Health regularly grant extensive funding to the School of Nursing and many of the Master’s programs in the School of Nursing are ranked first in the U.S.

The diabetes epidemic is growing in the U.S., and shows no sign of stopping: according to the 2011 National Diabetes Fact Sheet, 25.8 million Americans have the disease, with over 18 million diagnosed cases. An astonishing 79 million people have prediabetes, a risk factor in developing Type 2 diabetes—the most common form of the disease.

A retrospective study recently published in the journal “Arthritis Care & Research” reports that tumor necrosis factor (TNF) inhibitors could help prevent diabetes in patients with rheumatoid arthritis (RA), who commonly take TNF inhibitors to help in preventing joint disease.

The study, which was funded by Amgen/Wyeth, found that adults with RA who were treated with TNF inhibitors were much less likely to develop diabetes over the three to four year period following treatment over individuals who were not treated with TNF inhibitors.

“In RA patients, use of TNF inhibitors is associated with 51% reduction in risk of developing diabetes,” said Androniki Bili M.D., M.P.H., of the Center for Health Research at the Geisinger Medical Center in Danville, Pennsylvania. Dr. Bili served as co-author on the study. He did note that retrospective studies such as this one can only determine associations between conditions and cannot positively identify causation.

The study included data from 1881 adults who had been diagnosed with RA between January 1, 2001 and December 21, 2009. Patients who already had diabetes, of which there were 294, were excluded from the study. The researchers utilized proportional hazard regression models to adjust their findings to account for a variety of confounding factors, including age, race, sex, body mass index, rheumatoid factor, and anticyclic citrullinated peptide antibodies.

After exclusions, data from 1587 patients remained. Of the cohort, 522 were users of TNF inhibitors; 91 patients had developed diabetes throughout the course of the study, among them 16 users of TNF inhibitors and 75 non-users. Diabetes incidence rates stood at 8.6 and 17.2 per 1000 person-years for TNF inhibitor users and non-users, respectively. After adjusting for covariates, researchers were left with a hazard ratio of 0.49 for users of TNF inhibitors as opposed to non-users.

“RA is a systemic inflammatory disease with major cause of death being cardiovascular disease due to accelerated atherosclerosis,” explained Dr. Bili. “Diabetes and metabolic syndrome are major risk factors for cardiovascular disease. Therefore, medications that treat both the joints and the cardiometabolic comorbidities of RA are highly desirable. Although not an official guideline, I believe that patients with RA and metabolic syndrome, insulin resistance, or [body mass index greater than] 25 kg/m2 (all risk factors for diabetes) might benefit from earlier initiation of a TNF-a inhibitor in an attempt to control the cardiometabolic comorbidities along with the joint disease.”

According to Dr. Bili, his team’s findings support the hypothesis that TNF-a plays an important role in pathogenesis of insulin resistance—or the onset of insulin resistance, which often precedes Type 2 diabetes.

The study was reviewed by Daniel Solomon, M.D., M.P.H., who had previously observed a similar decrease in diabetes risk for patients with RA who were treated with TNF inhibitors.

“The authors conducted an interesting set of analyses and came to similar conclusions as we did in a recent paper published in JAMA,” said Dr. Solomon, referring to his own similar findings. “Their data set includes some potentially important variables that our analyses could not include. Thus, this paper adds to the literature.”

However, Dr. Solomon warned that even though the studies demonstrated similar results, they did not warrant a conclusion that TNF inhibitors directly cause the reduced incidence of diabetes.

“While there is a biologic basis that may link the use of TNF inhibitors to a reduced risk of incident diabetes, 2 epidemiologic studies do not prove causation. It would be premature for doctors to incorporate these findings into their management of systemic rheumatic diseases. However, studies suggesting a link between TNF inhibitors and diabetes risk reduction speak to the inflammatory basis of diabetes and insulin resistance. This study should encourage other investigators considering immunosuppressive treatments for diabetes prevention and treatment,” said Dr. Solomon.

Researchers from the Stanford University School of Medicine have discovered that the artificial activation of an important molecular pathway could someday be used to treat various diseases. The pathway is responsible for decreases in the growth of cells that produce insulin, and is activated naturally as an individual grows older. The findings were published in the October 12 edition of the journal “Nature.”

The pathway being studied appears in both mice and humans. It is activated by the expression of a particular molecule called platelet-derived growth factor receptor, or PDGF-receptor for short. Expression of this molecule naturally decreases over time, as does the growth of beta cells in the pancreas, which release insulin that helps removes glucose from the bloodstream and transports it to cells where it can be used as energy.

Scientists have long known that the growth of pancreatic beta cells decreases dramatically over time. In young and newborn humans and animals, beta cell proliferation is abundant.

Another molecule known as Ezh2 appears to be involved in the pathway that reduces production of beta cells, as expression of the molecule decreases over time. Scientists were unaware, however, what caused the change in expression of Ezh2.

Researchers on the study discovered that, in juvenile mice, the expression of PDGF receptors was reduced in the islet cells of the pancreas in a similar pattern to that of the decreases in beta cell production.

Blocking the expression of PDGF receptors in young lab mice—two to three weeks old—caused decreases in Ezh2 production and the number of pancreatic beta cells than control animals whose PDGF receptors were not affected. The mice with reduced Ezh2 production also demonstrated slightly higher blood sugar levels than control subjects and could not remove glucose from the blood stream as effectively when they were given a high glycemic load, such as after a meal heavy in carbohydrates.

A lack of expression in PDGF receptors also affected fully-grown lab mice: their ability to replace beta cells was diminished when the cells were destroyed by a compound that the researchers administered to the animals. They also developed severe diabetes after their beta cells were destroyed.

“We’re hopeful that soon we might be able to manipulate this pathway in a therapeutic way in humans,” said Seung Kim, M.D., Ph.D., senior author of the study and a professor of developmental biology at Stanford University. Kim believes that scientists may one day develop a therapy that activates the pathway to promote the regrowth of beta cells or prevent their destruction.

“Perhaps by rekindling its expression and then activating it through a drug we could give in an injection or through some other route. This could be a kind of one-two punch against diabetes,” continued Kim.

If scientists can develop a therapy that promotes growth of beta cells, it could offer a new method of treating or preventing diabetes that differs from current therapeutics, which mostly focus on maintaining healthy blood glucose levels. Replacing pancreatic beta cells could allow the body to produce its own insulin to regulate blood glucose instead of relying on insulin injections or other medication to control blood sugar.

“This gives us a handhold onto a vaster problem: how to control human beta cell proliferation in a therapeutic way,”

Additionally, the researchers commented that they found other molecular patheways related to the loss of beta cells due to aging that have not yet been explored.

Metformin treatment has been shown in research to provide a significant decrease in risk of cancerous cell growth and thus a decrease in risk of cancer overall. A recent meta-analysis has confirmed that patients with Type 2 diabetes who undergo metformin treatment are similarly at a significantly reduced risk of developing colorectal cancer — a 37 percent decrease in risk. The results were published in the October 2011 issue of the journal “Diabetes Care,” the journal of the American Diabetes Association.

“The results indicate that metformin therapy was associated with an estimated reduction of 37% in the risk of colorectal cancer among patients with type 2 diabetes,” said the researchers on the project.

The meta-analysis was conducted at Shanghai Jiao Tong University in China and was headed by Zhi-Jian Zhang, M.D., Ph.D., with the department of epidemiology and biostatistics at the School of Public Health division of the university. Dr. Zhang’s research team pooled together the existing data from studies that investigated the effects of metformin treatment on colorectal cancer in patients with Type 2 diabetes. Information was pulled from the SciVerse Scopus and PubMed databases, comprising five studies that had been published between January 1966 and March 2011. In all, data from 108,161 patients was identified and used to analyze trends in metformin treatment as it related to risk of colorectal cancer in Type 2 diabetics.

The researchers found that metformin therapy was associated with significantly decreased risk of colorectal neoplasm when compared to patients who received non-metformin treatment (RR=0.63; 95% CI, 0.50-0.79).

The research team did not include one of the identified studies, which had been conducted on colorectal adenoma. After the exclusion of that study, the data of 107,961 diabetes patients remained, with 589 cases of colorectal cancer occurring during the follow-up periods of the four remaining studies. After the findings were adjusted to exclude the study on colorectal adenoma, researchers still found that metformin therapy was associated with significantly reduced risk of developing colorectal cancer (RR=0.63; 95% CI, 0.47-0.84).

The researchers stated that they did not find any evidence which would suggest significant heterogeneity across the studies (P=.30).

According to the research team, metformin may help fight the growth of cancer cells due to its role in the tumor suppressor pathway, where it activates AMP-activated protein kinase (9) and is also a part of the sequence that activates LKB1, a gene that is known to suppress tumors. Additionally, in vitro studies have shown that metformin actually selectively kills cancer stem cells. Those findings have been confirmed in rodent experiments, which also showed that metformin inhibited carcinoma growth in the colon.

The authors noted that previous research has tested the effects of metformin on non-diabetic humans with rectal aberrant crypt foci — one of the earliest warning signs that the individual may develop colon cancer. The findings of that study demonstrated that one month of metformin treatment was associated with a decrease in aberrant crypt foci compared to a control group who did not receive metformin treatment.

The researchers commented that if metformin therapy is definitively proven in further research to significantly reduce risk of colorectal cancer, it will likely be prescribed to most diabetics as a measure to manage blood glucose levels and also to prevent cancer.

“If metformin therapy ultimately proves effective on reducing the risk of colorectal cancer, it would likely be recommended for the overwhelming majority of diabetes patients for both blood glucose control and cancer prevention,” said the researchers.

A recent population-based study conducted by researchers at Columbia University in New York found that patients who had been diagnosed with diabetes for a period of ten years or more were over three times more likely to suffer ischemic stroke. The study, called the Northern Manhattan Study, was a large, longitudinal investigation that allowed researchers to study how risk changed over long periods of time.

Scientists have known for years that patients with diabetes are at an increased risk of ischemic stroke. However, according to Dr. Julio R. Vieira, who presented the findings at the meeting of the American Neurological Association, the ten-year length of the study allowed researchers to look at long-term risks.

The study followed 3,298 participants of varied ethnic backgrounds. The participants had no prior history of stroke. They were tested for diabetes at baseline — the beginning of the study — and then tested again every year, starting in 1993.

The mean age of the participants at the beginning of the study was 69 years, with the ages ranging from 59 to 79. Over half of the participants were Hispanic, while 24 percent were black and 21 percent were white.

At the start of the investigation, 717 patients — 22 percent — had diabetes. An additional 338 patients (10 percent) developed diabetes throughout the course of the study.

Median follow-up among the participants was nine years. Throughout the follow-up period, 244 participants were diagnosed with ischemic stroke.

Researchers used Cox proportional hazards models to determine that the participants who had diabetes at the outset of the study were 2.5 times more likely to experience ischemic stroke throughout the course of the study. Additionally, the risk of suffering an ischemic stroke increased throughout the ten-year follow up period for patients who had diabetes at baseline as well as those were diagnosed with the disease during the study. Participants who had diabetes for five years or less increased their risk of ischemic stroke to 70 percent; those who had diabetes for five to ten years had an 80 percent risk of stroke; and patients who had diabetes for ten years or more were 3.3 times more likely to have an ischemic stroke.

Dr. Vieira stated in an interview conducted after his presentation that most of the participants involved with the study had been diagnosed with Type 2 diabetes. He noted that although diabetics were at an increased risk of ischemic stroke even from the beginning of the study, that risk did not triple until the patients had diabetes for ten years. Risk of stroke was always higher in diabetics but it took a fairly long history of the disease before the risk was significantly elevated.

“Diabetes, like hypertension and all of the other risk factors for cardiovascular disease, takes a while to really cause big damage,” said Dr. Vieira. “That’s exactly what we’re seeing here.” He stressed that patients who had been newly diagnosed with diabetes still had time to make changes to reduce their risk of stroke. “You have a lot of time for intervention,” he said.

However, the risk of stroke may be what compels diabetics to begin managing the disease more effectively. Dr. Vieira commented that even though he warns diabetics of the complications that can occur as a result of the disease, including vision loss and limb amputation, it doesn’t always incur changes. Significantly increased risk of a disabling or fatal stroke, however, may be the catalyst that drives diabetics to better manage the disease.